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Clinical Therapeutics 2 > Week 6 - Cardiovascular > Flashcards

Week 6 - Cardiovascular Flashcards

1
Q

Acute Pericarditis

A
  • Pericardium (inflammation of the outer layer of the heart) roughened, possible exudate
  • Sudden chest pain
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2
Q

Pericardial Effusion

A
  • Accumulation of fluid in pericardial cavity
  • Compression of heart may cause cardiac tamponade
  • Treated by pericardiocentesis (aspiration of fluid from the pericardial space)
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3
Q

Constrictive Pericarditis

A
  • Chronic inflammation of the pericardium with thickening, scarring, and muscle tightening.
  • Visceral and parietal layers adhere obliterating the pericardial cavity
  • Compress the heart CO (down)
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4
Q

Aortic stenosis

A
  • Diminishes blood from LV into aorta

* Result in ischemia, arrhythmias and heart failure

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5
Q

Mitral stenosis

A
  • Impaired blood flow from the LEFT atrium to the LEFT ventricle
  • Valve leaflets become and fibrous and fuse, chordae tendineae shorten
  • Atrial arrhythmias and thromboemboli
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6
Q

Aortic regurgitation

A
  • Inability of the aortic valve leaflets to close properly during diastole
  • Backflow of blood into LV causes it to dilate and hypertrophy
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7
Q

Mitral regurgitation

A
  • Backflow of blood into LA causes atrium to dilate, LA pressure
  • LV dilate and hypertrophy to maintain CO
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8
Q

Mitral valve prolapse syndrome

A
  • Valve cusps billow upward into atrium

* Replace with porcine or mechanical valve

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9
Q

Infective Endocarditis

A
  • Inflammation of the endocardium
  • Agents; Bacteria (staph or strep), viruses, fungi, and parasites in blood
  • Endothelium damaged (valves)
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10
Q

Disorders of the Arteries: Arteriosclerosis

A
  • Chronic disease with abnormal thickening and hardening of arterial walls
  • Smooth muscle cells and collagen migrate into Tunica intimata
  • Decreased elasticity
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11
Q

Disorders of the Arteries: Atherosclerosis

A

 Form of arteriosclerosis caused by accumulation of lipid-laden macrophages
 Results in plaque formation
 Is the main cause of CAD and CVA
 ½ deaths of western world
 Inflammatory disease initiated by injury to endothelium
 Injury from smoking, hypertension, diabetes,  LDL,  HDL, chronic infection

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12
Q

Atherosclerosis

A

 Clinical Manifestations
 Symptoms associated with inadequate perfusion of tissue
 Transient (intermittent claudication) or permanent
 Diffuse atherosclerosis will elevate systemic resistance and cause hypertension
 Major cause of MI and CVA

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13
Q

Evaluation and treatment of Atherosclerosis

A

 Reduction of risks
 Diet (most important contributor)
 Drugs can stabilise plaque before rupture (i.e. Aspirin: antithrombotic)

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14
Q

Aneurysm

A

 Localised dilation or out pocketing of a vessel wall or cardiac chamber
 Once initiated aneurysm grows bigger as tension in the vessel wall increases
 Can exert pressure on surrounding organs, rupture or dissect

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15
Q

Causes of an Aneurysm

A

 Atherosclerotic plaque erode and weakens tunica media
 Syphilis and other infections
 Chronic hypertension (50% of AAA)
 Marfans – inherited collagen vascular disease causes thoracic aortic aneurysm

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16
Q

True Aneurysm

A

* Involves all 3 tunica layers

Fusiform – entire circumference of vessel
Saccular – part of circumference, saclike

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17
Q

False Aneurysm

A
  • Initiated by break in tunica intima only
  • Extravascular haematoma as a result of graft leakage
  • Dissecting, saccular – blood entry causes longitudinal separation of vessel wall to form a blood-filled channel
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18
Q

Common sites of aneurysms

A
  • Aorta particularly susceptible

* Post infarct – stretching of non contractile muscle in heart

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19
Q

Clinical Manifestations

A

 Related to pressure on surrounding organs
 Most AAA asymptomatic
 Pulsating mass, calcified mass
 Pain is mild to severe mid-abdominal, lumbar or back region
 Stasis of blood favors thrombus and peripheral emboli

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20
Q

Dissecting Aneurysm

A

 Abrupt excruciating tearing pain
 Chest pain suggests ascending aorta; back pain descending aorta
 Dissection can be a life-threatening situation upon rupture

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21
Q

Dissecting Aneurysm Treatment

A

Risk of death depends on site of dissection
 Ascending aorta (type A) usually requires surgical repair with Dacron graft
 Descending thoracic aorta (type B) may be medically managed by aggressive control of BP and HR while aorta heals
 Once healed surgery may not be required

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22
Q

Intermittent claudication

A 
	Leg pain on ambulation due to atherosclerosis of iliofemoral arteries
	Dopplers to determine blood flow
	Vasodilators and antithrombotics
	Exercise rehabilitation
	Surgery
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23
Q

Thromboangiitis obliterans (Buerger Disease)

A
  • Inflammatory disease in male heavy smokers
  • Obliteration of arteries in hands and feet
     Pain, tenderness, Reynaud’s Phenomenon, cyanosis, redness and ulcers
     Gangrene
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24
Q

Reynaud’s Phenomenon and Disease

A

 Bilateral spasm in arteries and arterioles of hands
 Skin color and sensation changes
 Prolonged attacks affect cell metabolism in hands
 May be secondary to systemic disease i.e. scleroderma (excessive collagen deposition), smoking, exposure to cold or vibrating machinery
 Triggered by brief exposure to cold
 Common in young females
 Cause unknown

25
Varicose veins
* A vein in which blood has pooled  Distended, tortuous, and palpable veins  Caused by incompetent vein valve(s) and/or weakening of leg vein wall (collagen level)  Effects saphenous veins and perforating veins
26
Risk factors for Varicose Veins
 | * Genetics, age, gender, race, pregnancy (any hormone changes), obesity, diet, prolonged standing or sitting
27
Signs and symptoms of Varicose Veins
 | * Enlarged veins, leg swelling, painful legs, itchy legs, skin discolouration, thrombophlebitis
28
Treatment for Varicose Veins
* Self-care measures – leg exercises, support stockings, avoid high heels, avoid long periods of sitting or standing, elevate legs * Medical or surgical – remove or close off varicose vein i.e. sclerotherpy, laser, ambulatory phlebectomy, vein ligation and stripping
29
DVT
* Accumulation of clotting factors and platelets in deep leg vein  Promoting factors  Venous stasis (immobility, age, CHF)  Venous endothelial damage (trauma)  Hypercoagulable states (pregnancy, hormone replacement)
30
Thrombus
* Blood clot that remains attached to vessel wall  Develops where conditions promote activation of platelets and coagulation cascade  Intimal irritation and roughening (atherosclerosis)  Inflammation  Infection  Blood stasis (economy flights, aneurysms, phlebitis)  Trauma  Calcified areas or bacterial vegetations on heart valves
31
Treatment for Thrombus
* Anticoagulants to stop further growth of thrombus (Heparin or Warfarin)  Aspirin (antiprostaglandin) blocks platelet aggregation and platelet plug formation  IV and Intra-arterial Streptokinase to dissolve clot  Balloon-tipped catheter can pull thrombus out
32
Embolus
```  A bolus of matter circulating in blood  Thromboemboli  Air bubble (IV line or chest trauma)  Aggregate of amniotic fluid  Foreign substance (IV line or trauma)  Aggregate of fat (long bone trauma)  Bacteria (SBE)  Cancer cells ```
33
Hypertension
* Sustained elevation of systemic arterial BP;  Systolic > 120 mmHg Diastolic > 90 mmHg  Sustained diastolic pressure can lead to CHF, infarction, end-organ damage
34
Types of Hypertension
* Primary – 90-95 % are of unknown origin * Secondary – due to a primary disease * Isolated systolic – elevated systolic and normal diastolic
35
Factors associated with Primary Hypertension
 Family History  Gender and Age  Black race  High sodium intake  Low intake of potassium, calcium, or magnesium,  Diabetes mellitus  Smoking and obesity  Heavy alcohol consumption  Pathophysiology  Genetic susceptibility and environmental factors cause neurohumoral dysfunction, inflammation and insulin resistance  Causes  peripheral resistance and  blood volume
36
Secondary Hypertension
* Systemic disease process which CO and PR ``` - Renal - Endocrine - Vascular - Pregnancy - Drugs  Fix or remove disease and BP resolves ```
37
Complicated Hypertension
* Chronic damage to systemic blood vessels * Hypertrophy and hyperplasia of smooth muscle cells in arterial walls with associated fibrosis leads to ‘vascular remodeling’ * Results in reduced blood flow and organ dysfunction
38
Malignant Hypertension
* Hypertensive emergency where diastolic > 140 mmHg. | * Can cause encephalopathy (cerebral oedema)
39
Preeclampsia or toxemia
 After 24th week of pregnancy  Occurs in 6% of pregnancies, risk ^ age  Acute hypertension, proteinuria and oedema  Affects metabolism, renal function, CNS, fluid, electrolyte imbalance and may result in eclampsia (convulsions/coma)  Cause unknown  Resolves with birth of baby
40
Antihypertensive drugs
 Beta blockers  Atenolol, Metoprolol  Diuretics  Hydrochlorothiazide, Spironolactone  ACE inhibitors  Captopril  Calcium channel blockers  Nifedipine, etc  Centrally-acting drugs  Clonidine  Vasodilators  Hydralazine
41
ACE Inhibitors
 Angiotensinogen is produced constantly by the liver  Low renal blood flow (low BP), low sodium and/or potassium levels and β-adrenergic stimulation (adrenaline type stimulation) all cause renin release from juxtaglomerular cells in the kidneys  Renin converts Angiotensinogen to Angiotensin I  ACE, produced constantly in the lungs, converts Angiotensin I to Angiotensin II  Angiotensin II effects aldosterone secretion, smooth muscle constriction, Na+ and water retention  ACE inhibitors prevent conversion of Angiotensin I to Angiotensin II  End Results:  Decrease fluid retention, afterload  Example: Captopril
42
Captopril
``` Indication  Hypertension, heart failure Adverse Effects  Hypotension, angioedema (head, neck, intestinal), hyperkalaemia, proteinuria, cough; GI upset Practice points  Give small test dose  Monitor serum electrolytes ```
43
Postural/Orthostatic Hypotension
 Drop of 20 mmHg systolic BP or 10 mmHg diastolic BP within 3 minutes of standing  Vasodilation and blood pooling in muscles, spleen and kidneys  Results in dizziness and blurred vision
44
Acute Hypotension
 Sympathetic vasoconstriction mechanisms sluggish  30 to 50% of elderly, pregnancy and immobility (venous pooling)  Circulatory shock
45
Chronic Hypotension
Secondary to disease or poor nutrition
46
Treatment for Idiopathic Hypotension
```  Liberalization of salt intake  Raise head of bed  Slower position changes  Support stockings  Volume expansion  Vasoconstrictors ```
47
Dyslipidaemia
The Problem: * High serum levels of cholesterol- and/or triacylglycerol molecules * Thought to contribute to atherosclerotic disease  Solutions:  Decrease lipoprotein synthesis (bile acid binders)  Increase lipoprotein catabolism (fibrates)  Increase cholesterol removal (statins)
48
Niacin
Inhibits lipolysis in fat cells
49
Acute Rheumatic Fever and Rheumatic heart disease
* Inflammation of joints, skin, nervous system and heart | * Treatment - antibiotics - 9 days
50
Infective Endocarditis
* inflammation of the endocardium (inside lining of the heart) * Treatment - 4-6 weeks antibiotics/ repair or replacement surgery
51
Dissecting Aneurysm
* Abrupt excruciating tearing pain
52
Dyslipidaemia
* high levels of cholesterol/ triacylglycerol molecules
53
Simvastatin
Inhibit liver enzymes
54
Colestipol
Binds to bile salts
55
Statins
* Lower the rate of cholesterol production Adverse E: Stomach cramps, muscle/joint pain, rash, nausea and vomiting and constipation * Hepatitis * More effective at night * Short half lives, once daily admin
56
Heparin
Occurs naturally in the body | Prevents fibrin clot
57
Warfarin
Antagonist to Vit K Reversed with Vit K
58
Thrombolytics
* Given to dissolve thrombi
59
Abdominal Aortic Aneurism
Enlarged area of the lower part of the aorta Types: o Ascending: present with chest pain and require surgical correction o Descending aorta: presents with back pain. Can be managed by medication to stabilise BP and HR.

Clinical Therapeutics 2 (9 decks)

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